In the following ethanol is simply referred to as alcohol.
The drinking of alcohol is probably the oldest form of drug-oriented behaviour, dating back to the beginning of civilization. During the past few decades, a large variety of treatment procedures and treatment modalities were developed in the hope of controlling problem drinking. Such treatment procedures include the use of categories of drugs such as tranquilizers and anti-anxiety agents, anti-depressants, and mood-altering drugs. Another approach employed aversion-inducing drugs such as disulfiram (Bourne et al., Quarterly Journal of Studies on Alcohol, 27, 42-48, 1966) (disulfiram is also known under the trademark Antabuse.RTM.) or citrated calcium carbimide (Mellor et al., British Journal of Addiction, 66, 123-128, 1971) (Temposil).
It is however known that such punishment is an ineffective means of modifying behaviour, and that pitting a competing behaviour against an existing drinking behaviour will also be an ineffective method of altering behaviour because of response competition. This leads to the conclusion that the primary task in developing an effective treatment procedure will be to extinguish rather than punish the drinking behaviour. In other words, the aim is to permanently alter behaviour, and not merely temporarily suppress an undesired response. There are, however, very few reports, if any, which have used an extinction technique for the treatment of alcohol. Attempts to extinguish alcohol drinking must, by definition, succeed in breaking the contiguity between performance of this act and its positive reinforcement. However, in the case of alcohol drinking, this has been a difficult if not impossible task. The primary reason for this difficulty is the fact that alcohol serves as its own reinforcer. In other words, the drinking of alcohol is reinforced by the drinking of alcohol.
In recent years, development in neurochemical techniques and in research on the physiological and biochemical basis of motivation and reinforcement produced data which may give us a channel through which it may become possible to separate the act of drinking alcohol from the reinforcement produced by this act. The term "reinforcement" refers to the process by which the frequency of a response is changed as a function of the contiguity between the response and its consequences. Certain behavioural events or environmental objects are called reinforcers because it has been observed that under the proper conditions they are highly efficient modifiers of behaviour. A widely held notion is that alcohol (and several other drugs) has positive reinforcing properties.
Since the discovery and anatomical definition of the catecholamine-containing central nervous system neurons numerous studies have been published which lend support to the notion that catecholamines are involved in the mechanisms of positive reinforcement.
It has been suggested that catecholamines may be involved in the reinforcing aspects of drug self-administration. Pozuelo et al., (Mayo Clinic Proceedings, 47, 621-628, 1972) demonstrated that treatment with alpha-methyl-paratyrosine (an inhibitor of catecholamine synthesis) blocked the self-administration of morphine in monkeys. Meade et al. (Paper presented at the meeting of the American Psychological Association, New Orleans, 1974) found that pretreatment with 6-hydroxydopamine (a neurotoxin which selectively destroys catecholamine-containing neurons) blocked the oral intake of morphine in rats. One must conclude that the disruption of drug self-administration seen following catecholamine depletion is due to an interference in the capacity of the animal to perceive the rewarding properties of the administered drugs.
Several recent studies suggest that the integrity of the catecholamine systems of the brain is important for the maintenance of alcohol self-administration as well. To illustrate, Amit et al. (Psychopharmacologia, 17, 367-377, 1970, and ibid. 21, 317-327, 1971) showed that electrical stimulation of the lateral hypothalamus (a catecholamine-containing region of the brain) elevated ethanol intake levels in rats. Furthermore, Kiianmaa et al. (Neuro-science Letters, 1, 41-47, 1975) and Myers et al. (Research Communications in Chemical Pathology and Pharmacology, 10, 363-378, 1975) reported that depletions of catecholamine produced by 6-hydroxydopamine modified ethanol consumption in rats.
Collier (British Journal of Addiction, 67, 277-286, 1972) suggested while examining the nature of the effect of disulfiram on alcohol drinking that it is possible that disulfiram exerts its effect via its capacity to interrupt the catecholamine metabolism. This notion is somewhat contrary to the commonly held view that the main effect of disulfiram stems from its inhibitory action an aldehyde dehydrogenase (which produces elevations in blood acetaldehyde levels and subsequently a toxic reaction).
Although some references thus suggest that alcohol-oriented behaviour may be modified by manipulation of the catecholamine systems, these suggestions have not hitherto led to a successful method of controlling alcohol drinking.